RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis. - Wikidata - awgldk - TriplyDB

RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis.

RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis.

http://www.wikidata.org/entity/Q37071117

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Structure of the AML1-ETO eTAFH domain-HEB peptide complex and its contribution to AML1-ETO activity.Structure of the AML1-ETO NHR3-PKA(RIIα) complex and its contribution to AML1-ETO activity A stable transcription factor complex nucleated by oligomeric AML1–ETO controls leukaemogenesis AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemia CBFbeta is critical for AML1-ETO and TEL-AML1 activity.Genetic manipulation of AML1-ETO-induced expansion of hematopoietic precursors in a Drosophila model RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1).MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome.RUNX1 mutations in clonal myeloid disorders: from conventional cytogenetics to next generation sequencing, a story 40 years in the making The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.Myeloid translocation gene 16 is required for maintenance of haematopoietic stem cell quiescence.Combined gene expression and DNA occupancy profiling identifies potential therapeutic targets of t(8;21) AML.Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Core binding factor at the crossroads: determining the fate of the HSC.New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Chromosomal aberrations and fusion genes in myeloid malignancies.A role for RUNX1 in hematopoiesis and myeloid leukemia.Role of RUNX1 in hematological malignancies.RUNX1/ETO blocks selectin-mediated adhesion via epigenetic silencing of PSGL-1.Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Interference with RUNX1/ETO leukemogenic function by cell-penetrating peptides targeting the NHR2 oligomerization domain.Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.RUNX1 and CBFβ Mutations and Activities of Their Wild-Type Alleles in AML.RUNX1-ETO Leukemia.A novel exon in AML1-ETO negatively influences the clonogenic potential of the t(8;21) in acute myeloid leukemia.

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P2860

RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis.

http://www.wikidata.org/entity/Q37071117

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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name

RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

@en

RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

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type

label

RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

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RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

@nl

prefLabel

RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

@en

RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

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BLOOD-2008-04-153742

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P1476

RUNX1/AML1 DNA-binding domain ...... to AML1-ETO9a leukemogenesis.

@en

P2093

Dong-Er Zhang

http://www.w3.org/2001/XMLSchema#string

Eun-Young Ahn

http://www.w3.org/2001/XMLSchema#string

Ming Yan

http://www.w3.org/2001/XMLSchema#string

Scott W Hiebert

http://www.w3.org/2001/XMLSchema#string

P2860

The tetramer structure of the Nervy homology two domain, NHR2, is critical for AML1/ETO's activity

Identification of AML-1 and the (8;21) translocation protein (AML-1/ETO) as sequence-specific DNA-binding proteins: the runt homology domain is required for DNA binding and protein-protein interactions

The MYND motif is required for repression of basal transcription from the multidrug resistance 1 promoter by the t(8;21) fusion protein

ETO, a target of t(8;21) in acute leukemia, makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain

Oligomerization of ETO is obligatory for corepressor interaction

Multiple regions of ETO cooperate in transcriptional repression.

t(8;21)(q22;q22) Fusion proteins preferentially bind to duplicated AML1/RUNX1 DNA-binding sequences to differentially regulate gene expression.

AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations

E protein silencing by the leukemogenic AML1-ETO fusion protein.

Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts.

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883-886

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10.1182/BLOOD-2008-04-153742

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23500513

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19036704

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2630273

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